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Discussion Starter · #3 ·
Breeding- the dog or pedigree

All dogs carry defective genes. These defective genes are usually "recessive" - that is, their expression can be covered up by the presence of a normal gene for that function. It is estimated that the average dog carries 4 to 7 defective genes in it's DNA. (The human estimate is 10 to 12). Since genes are always carried in pairs, most of these abnormal genes are carried in a only single dose, so that their presence is completely concealed by the other, normal gene.

What is a gene?

A useful analogy is that a gene is like a set of instructions given to a particular workman doing a small job on a very big construction site. Each workman gets two sets of plans. If one set is damaged, he still has one good set, and the job can proceed. But if both sets are damaged, the job will not be finished, or it will be done wrong. A gene is a large molecule, a long double strand of DNA, composed of a backbone of two long sugar molecules linked by pairs of smaller molecules called "bases" or "nucleotides". It is the sequence of these nucleotides that encodes the information contained in the gene.

How does a gene become defective?

During normal cell division, an exact copy is made of each and every gene in the cell, and then it divides into two daughter cells which are each an exact copy of the original cell. Defective genes are caused by a "mutation". If something happens to disrupt the exact replication of the DNA during cell division, a defective gene results. Only a few changes in the base sequence can render the information in that gene useless. The process of aging is undoubtedly the effect of accumulated random defects of this sort, as are most types of cancer.
In the formation of egg and sperm, a special type of division takes place. Instead replicating the genetic material, so that both the daughter cells have a full complement of genes (two genes of each type), the genetic material is divided, so that each reproductive cell has only one gene of each type. When sperm and egg finally meet, the full complement of genes is restored, and a new individual, carrying half of its mother's genes and half of its father's genes is created.

Selective breeding.

Nearly all breeding of domestic animals is selective as opposed to random. Years ago, before the era of scientific genetics, breeding was done more by phenotype than by pedigree. Race horses tended to be bred by the stopwatch. That was where the money was. Dairy cattle were bred by the volume and quality of their milk, meat animals, by the speed of maturation and ratio of feed to meat, and so on. Later, it was recognized that breeding together closely related animals tended to speed up the process of "fixing" the desired traits within a few generations.

Breeding by pedigree

is the type of selective breeding most often practiced today. It nearly always involves some degree of inbreeding. The logic is simple. We know that an animal's traits are genetically controlled. We can even calculate the percentage of a particular animal's genes residing in the cells of one of its descendants. When we mate closely related animals whose family shows (has the phenotype of) the desired trait, we are reasonably sure it will appear in the offspring. Some breeders have carried this practice to remarkable extremes, failing to realize there is a "catch" to the pedigree method.

What about those defective genes?

The ones you can't see because they are "covered up" by intact ones. When we breed closely related animals, (let us say because they have super rears), we can see the desired trait. This trait is genetically controlled, like all traits. These two closely related animals share the genes for their super rears as a result of their close genetic relationship. What we can't see is the PRA gene or the kidney disease gene that these two animals also share as a result of their close genetic relationship. When we double up on the good rears we are also doubling up on the particular hidden defects they share.
We can see the results of this type of concentration of mutations in some human populations which have been relatively inbred by reason of isolation due to status, geography, or religion. Some examples that come to mind are Tay-Sachs disease in eastern European Jews, and hemophilia in some royal families.

Phenotype breeding

has been largely neglected in recent years. It has fallen into undeserved disrepute as the more popular inbreeding has produced faster and more dramatic changes. I say undeservedly, because it has much to recommend it, and avoids some of the serious pitfalls of inbreeding.
Again, we look at the phenotype of two relatively unrelated animals. They both have good rears, which we want. Why do they share this trait? For the same reason that the two related ones did: they both have the set of genes which produce good rears. But what about hidden, bad genes? Since these animals could not have been selected for unseen characteristics, (after all, if you can't see it you can't consciously select for it), they probably do not share many of these defective genes. To be sure, they still carry their load of defects in their own private collections, but they most likely each carry a different set. This being the case, it is very unlikely that any one offspring will inherit two copies of the same defective gene. It is very likely, however, that they will all have good rears.

Phenotype breeding is still selective breeding.

We are selecting those animals which show the desired traits, while minimizing the probability of doubling up on hidden, undesired ones. Inbreeding and linebreeding, on the other hand, selects for both the phenotypic and genotypic traits, and dramatically increases the probability of producing animals homozygous for defects. The lesson in all of this is that we should pay less attention to pedigrees, particularly in terms of looking for similarities on paper when we breed, and more attention to the dogs themselves. All too many breeders make their breeding decisions on paper, and not in the flesh. We need to consider the pedigrees as they relate to the qualities of the parent animal - did his mom and dad have good rears - rather than to insist he be related to our prospective brood bitch. We can get the results we want by breeding unrelated "like to like", without the tragic by products of inbreeding.

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Discussion Starter · #4 ·
Genetics and Breeding

Early geneticsWhen Mendel's work was rediscovered at the beginning of the twentieth century, the new field of Genetics went in several directions. The T. H. Morgan (1) school quickly got tired of crossing green to yellow peas and moved on to discovering white-eyed fruit flies, linkage and genetic maps. The Garrod (2) school started trying to figure out how genes controlled metabolism... and eventually everything else. The mathematically inclined, fearing to get their hands dirty, started thinking about how genes get shuffled around in a population. That led, around 1910, to the famous Hardy-Weinberg formula that relates the frequency of alleles to that of genotypes. For those unfamiliar with it, the basic formula assumes two alleles for a gene and sets the frequency of the first allele as p and that of the second one as q where p + q = 1. In a population that meets certain conditions, the relative frequencies of the three genotypes AA, Aa and aa will be p-squared, 2pq and q-squared. The main conditions are random mating, a large population, and no forces acting to change the allele frequencies.

This does not imply an endorsement of random mating, but was simply a starting point for the eventual development of equations to describe other situations. Most natural populations do not follow these rules. In nature, selection is often harsh, and most animals do not practice random mating. In many species that live in packs or herds, only the dominant male may breed and competition for that spot may be intense. Otherwise, the most common practice is probably assortative mating, where mates are chosen that have similar qualities (size, temperament, etc.) or are not closely related (negative assortative mating). How they decide on the latter is still being determined, but recognition of relatives probably depends on pheromones to a large extent.
Genetics without color

In the beginning, all geneticists held to much the same beliefs, or "model"- that there was one, and only one, good (or "wild-type") version of each gene. There were also a few nasty recessive mutants that would occasionally surface. They didn't really expect to find a large amount of diversity for most genes. They lived in a black-and-white world where genes were like light switches - either on or off, no in-between. As most of the bad mutations appeared to be recessive, good breeding was reduced to finding ways of efficiently identifying those carrying "degeneracies". Faith in inbreeding as a method for breeding the perfect individual was reinforced by various authors:
"Inbreeding... is a method of holding fast to that which is good and of casting out that which is bad. It establishes homozygous purity..." Onstott (1946)​
The morgan and garrod geneticists wanted nice "clean" mutations that were easily distinguished from the wild-type, and a population geneticist would never stoop to thinking about what a gene actually does! Their main concern was to figure out equations that would describe more complex situations involving selection, migration, and mutation, and explain what would happen to a new mutation give certain assumptions. Morphological variants, such as green and yellow peas, were not even really thought of in the same way. I mean, can you really think of a green pea as a "mutant"? (Or is yellow the mutant? How can that be if it is dominant?)

However, by the early '60s, if not before, those on the front lines were certainly aware of mutations that retained partial function ("leaky mutants"), even if they didn't want to work with them. By the '70s, the population geneticists actually started going out into the field and measuring the diversity in populations. They went in with the expectation of finding little difference between most individuals in a population and discovered far more than they had anticipated. The dust still hasn't settled completely. Logic suggested that if there was a considerable amount of genetic diversity, then there should be some reason for it. In a large population, the rare recessive mutation has little chance of gaining a toe-hold, and if it gets to the level where there are a noticeable number of homozygous mutants, selection will do its best to push it down again. Explaining diversity

Several theories were proposed, but somewhere along the line, the realization dawned that many populations are actually a loose collection of small populations that are semi-isolated. In a small population, random events take over and the frequencies of particular alleles may change dramatically just by chance ("genetic drift"). Given enough time, these random fluctuations generally eliminate all but one allele, which is said to be "fixed". How quickly this happens depends on how small the population is. Unequal use of individuals in the population increases the rate of allele loss because it decreases the effective population size.

Alleles with dramatic effects on viability are still generally selected against, but if the population includes several alleles of a particular gene, the "best" choice will not always be the winner. Sometimes an allele that reduces fitness by a small amount will take over. Over time, a small population may accumulate enough of these sub-optimal mutations for the impact to be noticeable.
Small populations also tend to become unintentionally inbred simply because there are not enough ancestors for each member of the current population to have a unique set (3). Neither intentional nor unintentional inbreeding lead to changes in allele frequencies, unless combined with selection, but they do lead to loss of heterozygosity. The decrease in fitness that results from accumulation of suboptimal recessives in the homozygous state is what we generally call "inbreeding depression". If there is an exchange of genes by individuals crossing over into another population's territory, the reduction in fitness due to gene loss will be reduced. The populations that we see in difficulty have often been cut off from other populations preventing this essential migration of genes. Canine examples include the Ethiopian and Mexican wolves, and the grey wolves on Isle Royale.

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Discussion Starter · #5 ·
The importance of breed originsSome breeds of domestic dog have evolved gradually over hundreds or perhaps even thousands of years. As most were bred for a purpose, some selection must have been involved. If you want a dog to guard your sheep, and it fails to do so, you are not likely to breed it. However, if you have two good herding dogs, you might breed them to each other, irrespective of their relationship. All the herding dogs in one valley may have been fairly similar and closely related, but exchanges would have occurred between neighboring valleys. If the population over a more extended region was bred for a common purpose, they might constitute a recognizable group, or breed, and it might acquire a descriptive name -- the Bavarian Sheepdog for instance. Such naturally-evolved breeds would be unlikely to have suffered major drift losses, even if they became locally inbred, because sufficient diversity would exist in the whole population, and there was no reason not to breed to a good sheepdog from another country. Whether one regards stud books and closed registries as good ideas or not, providing that sufficient numbers were admitted, such a breed should have at least started with sufficient diversity.

In contrast, when a breed is deliberately created from a small number of founders, the creator(s) generally concentrate first on inbreeding and selection to define the qualities they are after, rather than increasing the initial population and subsequently selecting for those that come closest to meeting their goals. Such a beginning generally removes most of the genetic diversity in the first few generations. If you have been unlucky or chosen badly, there may be little you can do.
The same fate may befall a naturally-evolved breed ( "landrace") if there is no recognized registry in the country of origin and too few founders are admitted into the registry somewhere else. At least in these cases, the potential exists of petitioning for reopening the stud book and admitting additional "founders". In those cases where there is no such reserve, the solution might be a merger with a closely related breed, or at least provision for some interbreed crosses. There are a few documented cases where this has been attempted in the last 20-30 years, but they have met considerable resistance. Don't shoot the messenger

Population genetics is not really a new discipline, it just seems that way because it's generally the last chapter in a genetics text. Population geneticists are neither white knights come to save us all, nor agents of the devil intent on destroying pure breeds. Population genetics is a tool for looking at an entire population or breed. It can tell you what has happened to the genetic diversity, and whether there is any possibility of improving the situation by making appropriate crosses. How this information is used is up to the breed club and individual breeders. Though lessons may be learned from conservation biology, I do not expect breed clubs are going to be in a position to manage the entire breed. However, they may choose to limit certain practices for the overall good of the breed. The prime target, in my opinion, should be overuse of popular stud dogs.

In a managed population of an endangered species, zoo biologists might choose one of several strategies that are generally aimed at conserving the diversity from the wild population from which the captive population is drawn. This makes the assumption that all founders were equally meritorious and that their genes are all equally worthy of preservation. This is essentially a holding action and, in the absence of selection, runs the risk of creating a population that is less well adapted to returning to the wild.
In my view, the best strategy for dog breeders is carefully planned assortative mating combined with an attempt to minimize or at least reduce the inbreeding coefficient. In practice, if I am asked for an opinion on a suitable mate for a Standard Poodle, I suggest that the breeder assemble a list of dogs he/she would consider breeding to, based on conformation, temperament and whatever other criteria are deemed relevant, and I will tell them the inbreeding coefficient for each potential litter and also about the prominent ancestors in the pedigree. My personal criterion is a 10-generation COI under 10%, but I might pick one close to that, or even a bit over, if I liked the other qualities. The COI has predictive value. I can tell you that an SP inbred to only 5% will, on average, live about 3 years longer than one bred to 35%, and I can tell you that a 10% increase will likely reduce litter size by about 7%. Both these effects are, in my opinion, most likely to result from accumulation of suboptimal alleles with small individual effects. However, inbreeding also increases the probability of doubling up on any obviously deleterious traits carried by a shared ancestor. I understand why breeders inbreed (or linebreed), but I don't agree that it is necessary to produce good dogs. As to the claim that it can be used to uncover problems in the line, I agree, but I can also give you case histories where the breeder has proceeded to ignore a hereditary problem uncovered this way, and as a result spread it through the breed.

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Discussion Starter · #6 ·
A Glossary of Genetic Terms
Alleles: different versions of the same gene (found at the same locus but in homologous chromosomes or in different individuals) that may produce different phenotypes.
Allele frequency: the fraction of all the alleles of a gene in a population that are of one type.
Assortative mating: a mating scheme that relies on the pairing of unrelated individuals with similar phenotypes to obtain consistency of type and reinforce desirable traits.
Codominant alleles: two alleles that have different effects that are distinguishable in a heterozygous individual (e.g. AB blood groups)
Cross-breeding: crossing two different breeds.
Dominant allele: one that determines the phenotype even when there is only one copy (i.e. in a heterozygous individual).
Drift: changes in allele frequencies over time due to chance (as opposed to selection or mutation).
Effective population size (Ne): the size of a hypothetical stable, randomly-mating population that would have the same rate of gene loss or increase in inbreeding as the real population (size N). As all finite populations are inbred to some degree and generally do not choose mates at random, Ne is typically 1/10 N or less, particularly if fewer males breed than females.
Epistasis: used to describe the situation where one gene's expression prevents the expression of another (e.g. you cannot determine whether an albino would have had black or brown hair, though these two traits are controlled by separate genes.)
Fitness (relative): The reproductive success of individuals of a particular genotype relative to the most fit genotype.
Fixation: loss of all alleles of a gene but one.
Founder: an individual drawn from a source population who contributes genetically to the derived subpopulation.
Founder effect: changes in allele frequencies that occur when a subpopulation is formed from a larger one. Typically many rare and usually undesirable alleles are excluded while a few carried by the founders get a big boost in frequency.
Founder equivalents: the number of hypothetical founders that would have the same diversity as the descendant population. Generally much smaller than the actual number due to unequal use and allele loss (gene dropping).
Gene: that portion of the genome that carries the information for a single protein. (In cases of proteins with multiple subunits, there may be a gene for each.)
Gene dropping: loss of alleles due to genetic drift.
Genetic bottleneck: when population numbers are temporarily reduced to a level insufficient to maintain the diversity in the population.
Genetic diversity: usually expressed in terms of percentage of genes that are polymorphic and/or are heterozygous.
Genome: the total genetic makeup of an organism.
Heritable: passed on from parents to progeny through the chromosomes/DNA.
Heritability: the fraction of the variability in a trait that is caused by genetic differences.
Heterozygous: carrying two different alleles of a gene.
Heterozygous advantage: a situation where the heterozygous genotype for a particular gene shows the highest relative fitness.
Heterozygous insufficiency: when the heterozyous genotype lacks sufficient gene product to have the normal phenotype. (Approximately equivalent to partial dominance.)
Heterosis: a situation where crossing two inbred lines yields progeny that are more healthy/vigorous than their parents. (More commonly used in plant breeding.)
Homologous chromosomes: in higher plants and animals, chromosomes are found in nearly identical "homologous" pairs, one coming from the sire and the other from the dam. A dog has 39 pairs, or 78 in total. Only one of each, chosen at random, is passed on through eggs or sperm to the progeny.
Linebreeding: a scheme that attempts to maintain a high contribution of one or two ancestors through successive generations. Often used by breeders for any inbreeding less intensive than between first-degree relatives.
Linkage: a measure of how frequently two genes found on the same chromosome remain together during gamete (egg or sperm) formation.
Locus: the location of a gene on a chromosome.
Map (aka linage map): a drawing showing the location of and relative distances between genes on a chromosome.
Mean kinship (mk): a measure of how related an individual is to the other members of a population. Generally computed as the average IC for the hypothetical progeny of the individual mated to all other members of the population (both sexes). A low average mk for a population indicates that most of the diversity carried by the founders has been retained.
Monomorphic genes: have only one common allele (rare alleles with frequencies of less than 0.001% may still occur).
Mutation: a change in the sequence of the base pairs in a DNA molecule.
Mutation rate: the number of new mutations that occur per gene per gamete per generation.
Outcrossing: mating two individuals of the same breed that are sufficiently unrelated that the IC of the progeny is lower than the average of the parents.
Polymorphic genes: have 2 or more common alleles in the population.
Recombination: the reciprocal exchange of portions of two homologous chromosomes (usually equivalent) during gamete formation.
Recombinant frequency (RF): how often two linked genes are separated by recombination, generally expressed as a percentage of total progeny.

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Discussion Starter · #7 ·
Eliminating Mutation, the Impossible Dream

Though it is not practical to eliminate all deleterious mutation, the incidence of affected individuals may be significantly reduced through a combination of intelligent breeding practice and the development of DNA tests.
Why do we have mutations?
Mutations are changes in an organism's DNA that potentially affect the correct functioning of genes. They occur naturally due to replication errors, mispairing of homologous chromosomes, or through unavoidable exposure to natural radiation (e.g., cosmic rays). Mutations can occur anywhere in the DNA and in any cell. They are heritable only when they occur in the germ cells (eggs and sperm), but mutations in the DNA of other (somatic) cells may lead to cancer. Even though the DNA replication enzymes are very accurate, and there are also supplementary systems for detecting and correcting damage, no system is perfect. We should, therefore, recognize that some level of mutation is inevitable. However, the mutation rate is increased by radiation, including ultraviolet light, and exposure to certain toxic chemicals. We can, therefore, take some precautions to minimize the risk..
The mutation rate for dogs cannot be determined readily, but from indirect evidence and extrapolation from other species, geneticists believe that mutation rates are normally on the order of 1 in 100,000 or less. For a sexually reproducing mammal, that would mean a new mutation in a particular gene would likely not occur more often than once in every 100,000 gametes. That may not seem like a high probability, but consider that most mammals are estimated to carry 80-100,000 genes. This suggests that every individual born has a good chance of carrying one new mutation in some gene.
What happens to new mutations?
Identical mutations are unlikely to occur simultaneously in the same gene from both parents (probability: < 1 in 10 billion), so any progeny will be heterozygous. (The exception being sex-linked genes, as the X and Y chromosomes are not homologous.) Dominant mutations will be expressed and any that are deleterious will be eliminated almost immediately from the population. If the mutation is advantageous, and this advantage is noticed by breeder or "nature", the mutation may survive and its frequency gradually increase. If a mutation neutral, which is to say, neither good nor bad (just different), its survival will be determined by "genetic drift". New recessive mutations remain hidden from selection until they reach a frequency where some homozygous individuals begin to appear. However, this does not prevent drift loss, which doesn't depend on phenotype.
Drift is a consequence of the random nature of genetic events. For example, if you breed a brown bitch to a black dog carrying brown, you would expect ½ the progeny to be black and ½ brown, but probably wouldn't be too surprised if you got 7 blacks and 3 browns in a litter of 10. It works the same way for any gene that has two or more alleles. Suppose that we have only one black dog (Bb), all the rest being bb. The one Bb dog may pass the B allele to none or all of his progeny, or to any number in between. If he has more than 5 black progeny, the frequency of black will go up providing all contribute equally to the next generation. In subsequent generations the frequency may drift even higher, or back down.
In a large population, the frequency will tend to fluctuate by only a small amount. However, small populations are inherently unstable and, if other factors don't intervene, one allele will eventually take over. This is called fixation. How long this takes depends on population size. With a rare breed, fixation may easily occur within 25 generations (~ 100 yrs.)
Many recessive mutations persist for a few generations at low levels before being lost again. Only very rarely do they reach a significant level in the population (> 1 in 1000). In terms of estimates of genetic diversity based on average heterozygosity, these genes are effectively monomorphic, as a screen of 50 or 100 individuals from the population would generally fail to reveal any differences for the majority of the these loci. When two individuals appear to carry the same mutation, it may well be due to independent mutations. However, unless there is some common ancestry, the chance of producing affected progeny should be no more than 1 in a million. [Notably, in the first study of an "inborn error of metabolism", Garrod (1902) observed that "among the families of parents who do not themselves exhibit the anomaly a proportion corresponding to 60 per cent are the offspring of marriages of first cousins." He estimates that only about 3% of all marriages are between first cousins.]
These estimates assume equal use of all individuals in the population, and we all know how common that is. If a particularly popular sire produces 10 times his "share" of sons and daughters, whatever deleterious allele(s) he carried will get a substantial boost in the next generation. A new mutation may be promoted from one-of-a-kind to moderately frequent in this way. As long as we insist on making mate choice a popularity contest, we risk introducing new problems as fast as we can develop tests for the old ones.
Genetic "load" and the founder effect
The human population carries at least 2500 deleterious mutant genes (or, more correctly, alleles of genes) causing significant health problems. For the most part they are fairly evenly distributed in the population. For the entire Canis familiaris population, the situation is likely fairly similar. Each individual is estimated to carry a "genetic load" of three or four "lethal equivalents", which implies recessive alleles that would kill of the bearer if they were homozygous. As long as they are recessive, they should not cause problems.
However, consider what happens if we form a subpopulation by choosing 10 individuals from a much larger population. Though these individuals will not carry the vast majority of the unwanted deleterious recessive alleles found in the wider population, the few they do carry will be promoted instantly from rare alleles (0.1% or less) to at least 5% in our example (or more generally, 1/2N, where N is the number of founders).
Because random drift has a greater impact on a small population, the population needs to grow rapidly, to at least several hundred breeding individuals, so as to minimize the loss of valuable alleles. During this time, we should select cautiously. While it is true that fixing "type" is one of the prime objectives of purebred dog breeders, too rigorous selection during the early generations increases the possibility of accidental loss of a valuable gene closely linked to one of the genes under selection. Dalmatians, for example, are all deficient in an enzyme required for correct uric acid metabolism. The mutant gene appears to be closely linked to one of the genes for the characteristic spotted pattern and was likely inadvertently fixed when early breeders selected for that pattern (Nash, 1990).

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Discussion Starter · #8 ·
Recognizing mutation
Though, at an allele frequency of 5%, affected individuals should only make up about 0.25% of the population, this would be a good time to stop it from increasing further. However, would a mutation occurring at that frequency be recognized as such? If we are talking about breed with average litter size of four, then we are only looking at about one litter in 100 with one affected puppy. If there have been no other reports, the breeder may simply write it off as "one of those things". In a breed with larger litters, the probability of two or more affected pups occurring in the same litter is greater, but even in these cases, lack of exchange of information between breeders and lack of education in genetics may result in a failure to identify the problem as genetic.
Selection is only effective if we are dealing with easily recognized phenotypes. However, undesirable mutations are not always that accommodating. There is a full range of possibilities from silent mutations, that have no noticeable effect on proteins coded for, to mutations that fail to make any functional product. There is even a small possibility of improvement. Those, and the silent class, are no threat to us. However, those that prevent normal function but do not eliminate it completely are likely to present a substantial problem. One example is the vWD mutation in Dobermans. This mutation eliminates 85-90% of the active clotting factor, but this low level is still sufficient to protect a homozygous affected individual from excessive bleeding in most situations. A dog that is "lucky" enough to avoid a major injury or surgery may not be recognized and may even be bred. Consequently, the frequency of the mutant allele rose to slightly over 50% in the population (Brewer, 1999).
This should not be regarded as an exception. Fewer than one in three mutations appear to be fully lethal, and that the others cover the full spectrum from the 0-100% activity. In addition to dealing with a handful of easily-recognized genetic diseases in a breed, we are also likely to be dealing with scores of others that reduce fitness but present no obvious phenotype that can be used to identify them. If we can miss a gene that is only 10-15% functional, how well are we likely to do with those that retain 80 or 90% of their normal function?
Why should this be a problem?
In a small population, drift inevitably leads to fixation for one allele. Computer simulations show that if we start with a neutral allele with a frequency of 5% in the population, as would be the case if it was originally carried by 1 of 10 founders, it will be fixed 5% of the time (surprise, surprise!). As the fitness of the homozygous phenotype decreases, its chances of being the winning allele decline. At a 5% reduction in fitness, 3.5-4% will still be fixed, most within 25 generations. At 15% the computer says the other allele will almost always win - if our slightly deleterious allele gets no boost from being linked to a selected gene or spread by a popular sire. However, one or both these conditions are usually violated, as discussed above. Furthermore, there is no guarantee that our selection will discriminate as finely as the computer.
If each such gene reduced fitness by only 5%, and the effects are additive, we could easily be facing a population with significantly lower litter sizes, shortened lifespans and greater susceptibility to non-genetic problems. Yet we would have no easily identifiable gene to pin it on.
Longevity and fertility, commonly regarded as indicators of "inbreeding depression", are reduced in canine populations which ave been inbred over a relatively short time period (Laikre and Ryman, 1991; Nordrum, 1994). However, most of the inbreeding in domestic dog populations does not appear to be due to breeders intentionally mating close relatives1 (though there are certainly exceptions), but to the loss of diversity due to drift and selection. The resultant loss of choices makes every individual a close relative, no matter what breeding strategy is employed.
The outcome for any breed will depend on both luck and on the breed's history. What is the effective population size? How many founders were there? Over how long a period prior to the closure of the stud books had the breed been refined? How intensive was the selection used to define type? Have there been any bottlenecks? How strong an influence have popular sires had?
What can we do?
1. We can control many of the obvious genetic diseases by supporting research aimed at locating the genes and developing direct DNA tests for the mutant alleles. Test results should be employed to make certain that carriers are only mated to clear individuals, rather than for wholesale elimination of carriers, which would further impoverish the gene pool.
2. We can explain to breeders that mutations will always be with us, and are not an indication of failure or bad breeding practice, and that an open exchange of information will produce the greatest rewards. We can also show them ways to achieve their personal goals without making choices that are detrimental to their breed.
3. We can attempt to educate breed clubs on the importance of maximizing diversity in the gene pool. As the keynote speaker at the recent AKC/CHF conference, Dr. Malcolm Willis, pointed out, few breeds even have a good idea of what their major genetic problems are, how many pups are in an average litter, or how long their dogs live. Fewer still have any idea of how to retain existing diversity or reduce the average inbreeding.

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Discussion Starter · #9 ·
the Nature of Genetic Disease.

Many people label any problem that appears to be inherited a "genetic disease." However, though there are legitimate genetic diseases, there are also a variety of problems that have an inherited component but are of a fundamentally different nature. Dealing effectively with any genetic problem requires an understanding of the relationship between the genes (genotype) and the phenotype. In many cases this is lacking. In this article, I would like to describe some of the differences, in order to give breeders and owners a better understanding of what they are dealing with. Inborn Errors of Metabolism: The true "genetic diseases"

The first clearly-described relationship between genotype and metabolic deficiencies is credited to Sir Archibald Garrod, an English physician. In 1901, he showed that the inherited disease alkaptonuria results from an inability to metabolize certain amino acids, leading to the accumulation of homogentisic acid. Some of this compound accumulates in skin and cartilage (the latter leading to arthritis). The rest is excreted in the urine, turning it black. Garrod suggested that the metabolic block was caused by an enzyme deficiency, though this was not confirmed until the enzyme (homogentisic acid oxidase) was characterized in 1958.
Since Garrod's time, many other inherited metabolic diseases have been discovered. Some can be managed by careful attention to diet; others cannot. A particularly nasty example is Tay-Sachs disease, which involves an enzyme important in lipid metabolism. Individuals homozygous for a deficiency in this enzyme accumulate a compound called a ganglioside in the nervous system. They appear normal at birth, but progressively lose motor function and die around three years of age. There is no treatment.
Most of these conditions involve mutations that lead to the production of a nonfunctional enzyme, or one that is totally absent. In heterozygotes, the single good copy of the gene is generally able to produce sufficient enzyme to handle the normal workload. However, in a few cases, carriers as well as affected individuals have to be careful about their diet or may exhibit less severe phenotypic effects.
Example of inherited metabolic diseases in dogs include phosphofructokinase deficiency in Cocker and Springer Spaniels, and pyruvate kinase deficiency in Basenjis.
Not all mutations involve metabolic pathways. Some involve proteins that have structural roles in cells and tissues. Others involve regulatory genes that control the correct sequence of events during development. These may lead to such problems as septal defects in the heart or the failure of the embryonic kidney to develop into the adult form. Nevertheless, all can legitimately be considered genetic diseases, as there is a direct one-to-one relationship between a single mutated gene and a particular problem. Conformational Diseases: The result of unnatural selection

Problems such as bloat (gastric dilatation-volvulus, or GDV) and hip dysplasia clearly have a genetic component, but also an environmental component and, perhaps, a behavioral one, as well (which also may be determined partially by the genes).
Bloat is not a "genetic disease" in the same sense as the metabolic and other disorders described above, and it seems unlikely that a single gene is responsible for bloat. One might better compare a bloat attack to a bad case of indigestion in a human. Some people are more prone to such attacks than others, and there may well be an inherited component, but other factors also come into play. Research into bloat suggests that diet, behavior, and conformation may all play a role.
Leaving aside the question of the role of genetics in behavior, the results suggest that the incidence of bloat increases with the size of the dog and the depth-to-width ratio of the chest cavity. This is a conformational problem, not a genetic disease. Certainly, the overall conformation is, ultimately, determined by the genes, but not by a single gene. There are probably dozens or hundreds of genes that go into determining the shape and size of the head, trunk, and limbs. Wherever there is genetic variability, one can select for larger, smaller, narrower, wider, etc. If the fancy as a whole decides that a taller, narrower dog looks more "refined," more of that description will be kept for breeding purposes, and the population will be shifted toward a more bloat-prone conformation.
When it comes to the question of correcting this problem, the solution, in theory, is simple. We stop breeding for a bloat-prone conformation and select for a slightly smaller dog with a chest cavity that is not so deep or narrow. Some may regard this as a retrogressive step, but we have to decide which we want to sacrifice.
I do not rule out the possibility that two dogs of identical conformation may have one or more genes that lead to one being more bloat-prone than the other. If we could identify these genes, we might be able to reduce the incidence of GDV somewhat while retaining some of the desired "refinement."
While it may be argued that there is nothing wrong with a tall, narrow dog aside from the greater risk for bloat, selecting for a conformation that is not functionally sound is a recipe for disaster. Wild canids do not move awkwardly. Any that did would be eliminated by natural selection. After thousands of years of evolution, the musculoskeletal system of the average wolf has found a combination that works efficiently. Because there is diversity in the gene pool, there is always the possibility of a chance combination of genes that produces an individual that can move more quickly and efficiently. There is also the possibility that a less efficient combination may arise, but it is not likely to be favored. In the artificial world of the show dog, one can insulate an individual from natural selection and favor a conformational extreme, because the breeder or the public thinks it looks more attractive or just different. Two such extreme dogs, bred together, may lead to something even more extreme and more popular. However, the changes in one component must be accompanied by changes in others, or the result, from a structural standpoint, may impose stresses that the components are not designed for. The result will be components easily damaged or deformed while the puppy is still growing. In such a case, one may not be dealing with genes that are "bad" and make a nonfunctional or defective product, just with a bad combination of genes. But if, during this "unnatural selection," the genes necessary to make a good combination have been discarded, where does this leave the breed?


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Discussion Starter · #10 · (Edited)
Significant Relationships

How would you determine the impact of a famous Champion on his breed?
A dog who has won many shows and earned many titles may have been quite popular as a stud and may have sired more winning progeny than other contemporary males. However, that does not guarantee that he will have more impact five or ten generations down the line than another dog who was bred only two or three times. Percent Contribution

If sufficient data is available, one way of determining the significance of an ancestor is to calculate his percent contribution to the current dogs. The % contribution (aka percentage of blood) is determined by the way genes are passed from the parents to the progeny. An individual inherits one set of chromosomes, and the genes they carry, from his or her sire and a second, homologous (equivalent) set from the dam. Thus, each parent makes a 50% contribution. As the parents in any generation always contribute 50% of their genes to their progeny, it seems reasonable to expect that 25% will come from each grandparent, 12.5% from each great-grandparent, and so on. However, once we are past the parents, we are dealing in probabilities, not certainties. This is not like mixing paint! When dad passes you one set of his chromosomes, they will include a selection of ones inherited from both his parents, but there is no guarantee that the selection will be exactly equal. There is even a small chance (very small) that he will pass on those from only one of his parents.
By the time we get back 10 generations, the contribution from each of the 1024 ancestors would, in theory, amount to slightly less than 0.1%. However, in the pedigree of the average purebred dog, there are seldom more than 100-200 different names and some appear 50 times or more. These are the significant ancestors that make the major genetic contributions.
If you have a pedigree, you can calculate % contribution of any repeats simply by multiplying the number of times each ancestor appears in any generation by the appropriate percentage for that generation and then add together all of the calculated percentage of contributions from each generation. The table listed below shows the percentage of blood inherited from each ancestor at the given generation levels. Generation "1" is the parents.
Genetic Contribution of Ancestors
Generation 1 2 3 4 5 6 7 8 9 10
% Contribution 50.0 25.0 12.5 6.25 3.125 1.563 0.781 0.391 0.195 0.098

You should get a number between 0 and 1; multiply by 100% to get the % contribution.
Databases exist for many breeds that will contain the data enabling you to extend a pedigree to 10 generations or more. Manual computation, though tedious, is still possible, but hardly convenient. Several pedigree programs (e.g. CompuPed) will quickly calculate % contribution for selected ancestors or all ancestors for a specified number of generations, providing you with information on which dogs have been most influential.
Inbreeding Coefficients

While most breeders recognize that a mating between half-sibs or cousins represents inbreeding, the majority probably have no idea which is the closer relationship. This is not helped by the non-standard definition of inbreeding in some books (e.g. Onstott's "Breeding Better Dogs").
The standard definition of inbreeding is that it is any scheme which results in the sire and the dam having common ancestors. Many breeders use the term "inbreeding" for close relatives and "linebreeding" for more distantly related individuals, but there is no fundamental difference.
The parameter used to express this common heritage is called the inbreeding coefficient and was first proposed by Sewell Wright in 1922. Designated F by Wright (but more commonly IC or COI by breeders), it can theoretically range from 0 to 100%, and indicates the probability that the two alleles for any gene are identical by descent.
The primary consequence of inbreeding is to increase homozygosity. However, the IC is not a direct measure of homozygosity because the two alleles passed down from different ancestors may be functionally the same. Furthermore, some proportion of all the genes will be the homozygous because there is only one allele. The IC serves as an indicator of what proportion of the remainder may have been made homozygous by inbreeding.
The inbreeding coefficient is a function of the number and location of the common ancestors in a pedigree. It is not a function, except indirectly, of the inbreeding of the parents. Thus, one can mate two highly inbred individuals who share little common ancestry and produce a litter with a very low IC. (Because the potential number of ancestors doubles every generation, eventually you reach a point where the number of ancestors exceeds the number of individuals alive at that time. You are, therefore, bound to find some common ancestors if you go back far enough.) Conversely, it is possible to mate two closely related dogs, both of which have low ICs, and boost the IC substantially. The most widely used approach for calculating inbreeding coefficients is Wright's "paths" method (see note), best illustrated by a simple example. Suppose we mate half-sibs, the common ancestor, Anson, being the father. Don is the son of Anson and Bess; Eva the daughter of Anson and Claire.
Fred is one of their progeny.

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Discussion Starter · #11 ·
To simplify, we don't show the ancestors that aren't shared:

Now we consider a gene for which Anson carries two different alleles, a1 and a2. There is a 50% probability of the allele Anson passed to Don being passed on to Fred. There is also a 50% probability that the same allele will be passed from Anson to Eva, and a 50% probability of it being passed from Eva to Fred, if Eva got it. When dealing with events that are contingent (this *and* that must happen), we multiply the probabilities - in this case 0.5 x 0.5 x 0.5 = 0.125 (12.5%). This final number is the probability that Fred will be homozygous for either a1 or a2 because of the common grandfather.
In general, Wright's method is to determine the path from Fred to the common ancestor, Anson, and back again on the other side of the pedigree (Fred-Don-Anson-Eva-Fred), count the number of individuals in the path, excluding Fred (there are 3, Don-Anson-Eva) and then calculate ½n, where n is that number. So, in the present case, we have (½)3 or (½ x ½ x ½) = 1/8, or 12.5%. If this were the only common ancestor, the inbreeding coefficient for Fred would be 12.5%.
Now, suppose the common ancestor was one of the grandfathers of the parents (i.e. a great-grandfather of the litter). This adds an individual on each side of the pedigree, so that we will get a path of the type Fred-X-Don-Anson-Eva-Y-Fred, and the inbreeding on Anson will be (1/2)5 or 1/32 (3.125%).
Like many other genetic calculations, the IC is based on probabilities, not certainties. An individual may be more or less highly inbred than the number computed.
If we had only a single common ancestor to deal with, life would be relatively simple. However, there are two complications to deal with. The first is that there will be more than one common ancestor. Let's consider the case of first cousins. In human populations such a pairing is prohibited in some societies but allowed in others. We have already calculated the inbreeding for a single shared grandparent. First cousins have two shared grandparents, and we simply add the inbreeding coefficient for each to get 6.25%.
The second complication is that the common ancestor may be inbred. If so, his or her inbreeding coefficient will have to be calculated. To account for this we have to multiply the inbreeding coefficient calculated for Fred by (1 + FA), where FA is the inbreeding coefficient calculated for Anson. For example, if Anson is the product of a mating of first cousins, the total inbreeding for Fred will be 0.125 x 1.0625 = 0.133 (13.3%) if there are no other shared ancestors in the pedigree.
Unfortunately, in the average pedigree, there are a large number of shared ancestors. Therefore, the total inbreeding for a dog cannot generally be calculated manually and appropriate software must be used (e.g. CompuPed). Calculating inbreeding for only the first few generations is not particularly useful. If there are more than one or two common ancestors in four or five generation pedigree, the inbreeding is probably already higher than desirable. Unfortunately, having none is no guarantee that common ancestors will not occur in abundance further back, and some pedigrees of this type still achieve moderately high inbreeding coefficients. Neither can be number of shared ancestors be used as a reliable guide, as the inbreeding coefficient is very sensitive to when and where they occur in a pedigree.

Is there a quick way of determining how genetically similar two dogs are?
Suppose a breeder has two bitches (A and B) she wants to mate to different males. After careful research she has identified three potentially suitable males (C, D and E), all of which look equally good. She hopes to get a male puppy from one litter and a female from the other, and would like to eventually breed them to each other. The objective could be to pick the combination that will minimize the potential inbreeding. Alternatively, she may be looking for two dogs that are not close relatives yet have similar heritage.
One approach would be to produce hypothetical litters for all combinations: AC, AD, AE, BC, BD and BE. Then we would have to look at the possibilities for the second generation. There will be six if we don't permit shared grandparents, and 36 if there are no restrictions. These potential litters could then be evaluated for inbreeding or the % contribution of significant ancestors. This will certainly provide the data, but is unnecessarily tedious. The Coefficient of Relationship

The coefficient of relationship (RC) provides a way of objectively assessing the similarity of two pedigrees by giving a number that is a direct measure of shared ancestry. In most human populations, two individuals picked at random would likely have a RC of 0, a brother and sister 50% and identical twins 100%. Other relationships would fall between 0 and 50%.

The number generated may be viewed as analogous to the % composition, except that you are comparing two dogs instead of looking at one. A brother and sister will give a value of 50% as long as an ancestor is not repeated. Once ancestors start to repeat, the individuals no longer have an inbreeding coefficient of zero. Two sibs from a highly inbred line may have an RC of 80% or more, and two dogs that are not sibs may have an RC above 50%.
The formula for the RC is:
RAB = 2fAB ÷ [(1 + FA)(1 + FB)]½
where fAB is the inbreeding coefficient of a hypothetical litter between A and B, and FA and FB are the inbreeding coefficients for the two individuals, A and B.
A simpler approach to the breeder's problem would be to compute the RCs for C vs D and E, and D vs E. This is not a pencil and paper calculation. However, presented with just such a problem, it took me about 2 minutes to obtain the three RCs with the latest version of CompuPed. My results were RCD 10.4%, RCE 13.4%, RDE 17.2%.
As D and E share the most common ancestry, so would the progeny from their two prospective litters, while C and D share the least. To minimize inbreeding and maximize diversity, they would be my choice, all else being equal. (These values actually all fall below the average for the breed, which is ~ 23%.) The Kinship Coefficient

The fAB term in the RC equation is sometimes called the "kinship coefficient" and may also be used as a measure of the relationship between two individuals. It's computation is the same as that of an inbreeding coefficient for a hypothetical litter between the two dogs. (It doesn't matter if they are the same sex.)

The mean kinship (mki) for individual i is is the average of the kinship coefficients (fij) between i and all the other breedable individuals in the population:

A conservation biologist would consider the individual with the lowest mean kinship to be the most genetically valuable in terms of maintaining diversity in the population, and would try to favor that individual in a breeding program.
Note: An alternative approach, often referred to as the "tabular" method, calculates inbreeding from the ealiest ancestor forward to the current dog (or dogs).

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Discussion Starter · #12 ·
Breeding Schemes

Breeders often talk about inbreeding and outcrossing as though they were the only possibilities -- and generally with negative comments about the latter. There are other possibilities, and I have long been a proponent of assortative mating. It is not a theoretical concept that doesn't work in practice; I know several breeders who do it and achieve good results. This essay will attempt to explain why it is a good idea, but first I need to define the alternatives.
Random Mating

Though random mating is not a common breeding practice, understanding what this implies is important. Random mating is exactly what the name implies: mates are chosen with no regard for similarity or relatedness. (If the population is inbred to some extent, randomly-selected mates may be related.)
Random mating is one of the assumptions behind the Hardy-Weinberg formula, which allows one to calculate the frequency of heterozygous carriers from the frequency of individuals expressing some recessive trait in a population. Because inbreeding among purebred dogs and in other small populations decreases the frequency of heterozygotes, these estimates may be higher than the actual incidence.
Inbreeding and Linebreeding

Inbreeding is the practice of breeding two animals that are related (i.e., have one or more common ancestors). The degree of inbreeding may be assigned a value between 0 and 1, called the inbreeding coefficient, where 0 indicates that the animals have no common ancestors. Because the number of ancestors potentially doubles with every generation you go back in a pedigree, you eventually get to a point, even in a very large population, where there are simply not enough ancestors. Thus, all populations are inbred to some degree, and a true outcross (the term generally used when two animals are "unrelated") is not really possible. The term is generally misused to describe a cross between two animals with different phenotypes.
In a population with a limited number of founders, a maximum number of ancestors -- the effective population size -- is reached in some past generation. This number will be governed by various factors, such as the total population size, how far individuals travel during their lifetime, and whether there are inbreeding taboos or other mechanisms that reduce the likelihood of close relatives mating.
Inbreeding does not change allele frequencies directly, but it does increase the proportion of homozygotes. Individuals homozygous for deleterious genes are likely to be removed from the breeding pool by natural selection (if they do not survive to reproductive age) or by man.
Linebreeding is merely a term used for a particular type of inbreeding that often focusses on one ancestor who was considered exceptional. Particularly if it is a male, this exceptional ancestor may end up as grandfather and great-grandfather -- sometimes more than once -- in the same pedigree. Father-daughter, mother-son, and some other combinations also result in a disproportionate number of genes coming from a single ancestor. This type of close inbreeding is less common. [In contrast, the mating of full sibs or first cousins doubles up on two ancestors equally.]
As the result of several common practices, most pure-bred domestic animals are more inbred than they really need to be. One is that some breeders own a small number of animals and breed only within their own group. A second is that many breeders have the idea that outstanding animals can be produced by inbreeding -- by doubling up on the good alleles while somehow avoiding the bad. Even if you were to point out that this is a gamble, such breeders might respond that they are simply helping natural selection.
Beyond the conventional close-relative inbreeding, there is another practice that has much the same effect, namely the popular sire phenomenon (generally over-use of a well-promoted champion). In fact, many who breed to such a dog believe they are doing a "good thing," as they will be increasing the frequency of occurrence of the genes that made him a champion. What they may not realize is that they are increasing the frequency of all genes carried by this animal -- whether they are good, bad, or innocuous -- and that champions, like any other animal, carry a number of undesirable recessive alleles (the genetic load) that are masked by wild-type alleles. The result of the popular sire phenomenon is that almost all members of the breed will carry a little bit of Jake Hugelberg, and any undesirable trait carried by Jake will no longer be rare. Finding a safe, unrelated mate then becomes an exercise in futility.
If we lived in a world where all the genes followed the simple rule that there may only be good alleles, which are dominant, and bad alleles, which are recessive, then inbreeding could be an effective tool for improving a breed. However, during the past 25 years, geneticists have been directly measuring genetic diversity in populations by looking at the DNA or proteins, rather than at the phenotype. They have found that many individuals who cannot easily be distinguished by their phenotypic appearance nevertheless have considerable differences in their genotype. Some of these alternative alleles (termed neutral isoalleles) are functionally equivalent. Others have lost only a small portion of their normal function.
Suppose we have a "mutant" allele that has lost only 5-10% of its normal function. In many cases, this would not produce a noticeable effect. If you made an individual homozygous for this allele, you would not even be aware that you had done so. Now consider that the same fate may befall a number of genes during an inbreeding program. Eventually, you will have an individual that is considerably less fit than one carrying the normal alleles for all (or even most of) these genes. There is no magic formula for regaining what you have lost. You must start again.
[Sometimes mutant alleles result in an even more dramatic loss of function, but remain undiscovered under normal conditions. A good example is vWD in Dobermans.]
About the only animals that are routinely inbred to a high level are laboratory mice and rats. There, the breeders start breeding many lines simultaneously in the expectation that the majority will die out or will suffer significant inbreeding depression, which generally means that they are smaller, produce fewer offspring, are more susceptible to disease, and have a shorter average lifespan. Dogs are no different. If you can start with enough lines, a few may make it through the genetic bottleneck with acceptable fitness. However, dog breeders generally don't have the resources to start several dozen or more lines simultaneously.
Sometimes two different alleles may be better than one. Consider the major histocompatibility complex (MHC). These genes are responsible for distinguishing "self" from "foreign", and a heterozygous individual can recognize more possibilities than a homozygous one. Having a variety of MHC alleles is even more important to population survival. Not only does this provide better defense against pathogens, but there is growing evidence that parents who carry different MHC haplotypes may have fewer fertility problems. This is not a universally accepted theory, but today one is hard pressed to find a conservation or zoo biologist concerned with preserving an endangered species who would not list maintaining maximum genetic diversity as one of his/her primary goals.

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Discussion Starter · #13 ·
Assortative mating

Assortative mating is the mating of individuals that are phenotypically similar. It is a normal practice, to some degree, for humans and various other species. Though phenotype is a product of both genotype and environment, such individuals are more likely to carry the same alleles for genes determining morphology. If we are talking about a conformation that is basically sound from the structural point of view, the genes involved will have been subjected to natural selection for thousands of years and will most likely be dominant. The major characteristics that set one breed apart from another will likely have been fixed early in the breed's history. ("Fixed" means that there is only one allele of present in the population. If there is only one allele, the question of dominance does not arise.) Consequently, when you look at a dog, you are looking at his genes. If the conformation (or, for that matter, the temperament, intelligence, or whatever) is not good, then you are very likely looking at a dog or a breed that is homozygous for one or more recessive alleles that you would probably like to get rid of. If it is the dog and not the breed, you may elect not to breed him, or you may look for a mate that covers the problem. If it is the breed, the only solution would be to introduce some genes from another breed. (That would be an outcross!)

Breeding together animals that share dominant good alleles for most of their genes will produce mainly puppies that also carry these genes. Even if the parents are not homozygous for all these good alleles, you should still get many that are suitable. More important, if animals heterozygous for certain genes are more fit, assortative mating will preserve more heterozygosity than inbreeding. However, unlike inbreeding, assortative mating should not result in an increased risk of the parents sharing hidden recessive mutations. Though we might like to eliminate deleterious recessives, everyone carries a few. Trying to find the "perfect dog" without either visible or hidden flaws is like betting on the lottery. There may conceivably be a big winner out there, but they are certainly not common.
The more you try to cover the deficiencies in one dog with good qualities in another, the less the dogs will have in common. If, then, the results are unsatisfactory, they should not be blamed on assortative mating, as that is no longer what you are doing.

The risks involved

Some traits that breeders consider desirable could be the result of homozygosity for a recessive allele for gene A or gene B. Obviously, crossing an AAbb with an aaBB will produce AaBb progeny that will not express this trait. (However, aside from some of the genes affecting coat color, I can think of no examples.)
If care is not taken to go back far enough in the pedigrees, you may have two animals with similar phenotypes resulting from common ancestry. Whether you are inbreeding unintentionally or intentionally, the consequences are the same. The solution is simple: check the heritage.
Because assortative mating involves selection (you are hopefully mating the best together, and not the worst), you are denying some dogs the opportunity to pass their genes on to the next generation. This is, perhaps, the subtlest of risks, as it does not seem to involve doing anything "wrong." Most would argue that it is merely doing what nature does -- eliminating the least fit. But what if some of these "less-than-best" happen to be the only ones to carry the best allele for some gene? Out goes the good with the bad!
This is primarily a "low-numbers" risk. The larger the population, the less likely we are to find that important alleles are carried by only a few individuals. However, it pays to know where the diversity lies. Do any of you know which, among the current dogs, are most likely to carry the genes of any given founder?


Inbreeding calculations do not account for the possibility that an allele will become homozygous by "chance," though this, too, can be calculated if the frequency at which an allele occurs in the whole population is known. Most basic Genetics texts explain how. (See, for example, Willis, pp. 293-295, "The Hardy-Weinberg Law.")
I have seen figures of 2500 genetic diseases in man and there are likely to be as many in Canis familiaris, taken as a whole. In man. the vast majority are rare (allele frequencies of < 0.01, which means < 1 in 1000 affected). However, everyone carries three to five "lethal equivalents." This is their "genetic load." Canine breeds are often established with a handful of founders, so we end up with a subset of one or two dozen problems, at frequencies at least 10-fold higher. [If we had five founders, each with a unique set of problems carried as single recessive alleles, the allele frequency of each will initially be ~ 0.1 and ~ 1% will be affected.
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